First, TC, you have to define "sugar." Are you suggesting that a diet
consisting of mostly fruit, with some good quality protein source in
the miniumum amount, is dangerous? Well, then, get some rats, feed
them this kind of diet, and see how long and how well they live
(assuming you are supplementing for truly essential vitamins and
minerals). In fact, it is arachidonic acid causing the problems, as
usual.

Too much of any sugar or refined or high-GI carb is unhealthy for
humans.

Remember that todays fruits have been modified either thru selective
breeding or direct genetic manipulation to be sweeter for the mass
markets. Todays fruits are not your grandparents fruits. And we
historically (over the millions of years we developed in the northern
lattitudes) never had access to such large amounts of them available
year round.

Chronic diseases have exploded in the last 30 years in spite of the
inceased availability and increased consumption of fruits. And there
have been a huge push for us to eat more fruits in the last 30 years.
Just check out the food pyramid. It seems to be recomendation number
one for us to eat more fruit, with the possible exception of the
constant mantra of more grains. Oddly enough, both of those commodities
are highly marketted and are huge money makers for multi-national
corporations.

And fruits are not the only food that contain vitamins. Real foods like
fresh meats and fresh lower-GI produce contain plenty of the nutrients
we need including fats, fat soluble vitamins, water soluble vitamins of
all kinds, and the proteins we need, including the all important
*essential* fats, proteins and vitamins. Somehow many people seem to
equate vitamins only to fruits, while ignoring the important nutrients
in other real foods.

Most of todays grocery store fruits are picked way before they ripen
and develop all their vitamin content. They are allowed to ripen in
transit, in storage or are forced to ripen just before delivery. The
huge time lag between picking and eating allows the fruits vitamin
content to diminish even more. Water soluble vitamins are sensitive to
time and heat and will degrade enormously over a period of a few days.
By the time you buy them, they have lost a lot of their water soluble
vitamin content. If all the fruit you eat is picked fresh from the
plant, then you will have some guarantee of some good amounts of
vitamins, but even then they will still be selectively bred to have a
higher sweetness content.

Your body will use up some vitamins in the process of metabolising
sugars. If your fruit is relatively low sugar and is very fresh and
contains lots of vitamins, there will be some left over for your body,
and you will be better nourished when you are done eating. If however,
the fruit is especially sweet and somewhat depleted or bereft of
vitamins, there will be less left over for your body. And if the amount
of vitamins needed to metabolise the sugars in the fruit is more than
the stale fruit contains, the body has to get the vitamins from your
bodies stores to metabolize the sugars, and the old stale overly
sweetened fruit will actually deplete you of vitamins. Now imagine
eating carbs and sugars with no accompanying fruit which contains these
vitamins. You are depleting your system of vitamins every time you eat
refined carbs. Hence, on a high carb diet you become malnourished and
will develop all kinds of chronic symptoms and disease.

Remember that bears fatten up on berries. Too much sweet fruit will
lead to obesity and obesity related disease regardless of how much
vitamin you think they contain.

Take any primarily carnivorous animal that you like and feed them your
test high fruit diet and see what happens. They will not be as healthy
as when they are eating a proper primarily meat diet.

First, TC, you have to define "sugar." Are you suggesting that a diet
consisting of mostly fruit, with some good quality protein source in
the miniumum amount, is dangerous? Well, then, get some rats, feed
them this kind of diet, and see how long and how well they live
(assuming you are supplementing for truly essential vitamins and
minerals). In fact, it is arachidonic acid causing the problems, as
usual.

I've cited this Fu, et al. study here before, and I will assume that
you have not read it,but it explains what is going on at the molecular
level. You can eat your sugar, if by that you mean a fruit that is not
too high in fructose in large amounts or if you mean something like
Rapadura brand, but stay away from the highly unsaturated oils:

J Biol Chem 1996 Apr 26;271(17):9982-9986

The advanced glycation end product, Nepsilon-(carboxymethyl)lysine, is
a product of both lipid peroxidation and glycoxidation reactions.

Fu MX, Requena JR, Jenkins AJ, Lyons TJ, Baynes JW, Thorpe SR

Department of Chemistry and Biochemistry and School of Medicine,
University of South Carolina, Columbia, South Carolina 29208, USA.

Nepsilon-(Carboxymethyl)lysine (CML) is an advanced glycation end
product formed on protein by combined nonenzymatic glycation and
oxidation (glycoxidation) reactions. We now report that CML is also
formed during metal-catalyzed oxidation of polyunsaturated fatty acids
in the presence of protein. During copper-catalyzed oxidation in vitro,
the CML content of low density lipoprotein increased in concert with
conjugated dienes but was independent of the presence of the Amadori
compound, fructoselysine, on the protein. CML was also formed in a
time-dependent manner in RNase incubated under aerobic conditions in
phosphate buffer containing arachidonate or linoleate; only trace
amounts of CML were formed from oleate. After 6 days of incubation the
yield of CML in RNase from arachidonate was approximately 0.7 mmol/mol
lysine compared with only 0.03 mmol/mol lysine for protein incubated
under the same conditions with glucose. Glyoxal, a known precursor of
CML, was also formed during incubation of RNase with arachidonate.
These results suggest that lipid peroxidation, as well as
glycoxidation, may be an important source of CML in tissue proteins in
vivo and that CML may be a general marker of oxidative stress and long
term damage to protein in aging, atherosclerosis, and diabetes.

ing for both lipid and protein using a Paragon LIPOEPG system (Beck-man
Instruments, Palo Alto, CA), which showed a single lipid and
protein band; contamination with albumin was not detected. LDL pro-tein
concentration was estimated by the method of Lowry (11). LDL
pools were prepared by combining LDL from three individuals.
To remove salts, EDTA, and water-soluble antioxidants prior to
copper oxidation experiments, LDL was chromatographed on PD-10
columns (Pharmacia Biotech Inc.) equilibrated in phosphate-buffered
saline (PBS; Ref. 12) that had been gassed with nitrogen. The LDL was
sterilized by ultrafiltration (0.22- mfilters, CoStar, Cambridge, MA)
and
then diluted to ;100 mg of protein/ml using PBS that had been bubbled
with oxygen for at least 10 min. The diluted samples were adjusted to
5 mM CuCl2 , placed in loosely capped plastic bottles, and incubated at
32 °C; copper was omitted in control samples. The progress of the
oxidation reaction was monitored by measuring absorbance at 234 nm
in aliquots removed at various times. For analysis of CML, aliquots (;1
mg of protein) were adjusted to 1 mM in diethylenetriaminepentaacetic
acid (0.1 M) in sodium borate, pH 9.2, and reduced overnight at 4 °C
with a final concentration of 25 mM NaBH4 . The samples were then
dialyzed against water, dried by centrifugal evaporation (Savant
Speed-Vac,
Farmingdale, NY), and delipidated using methanol:ether (3:10)
(13). For analyses of FL, samples were treated with
diethylenetriamine-pentaacetic
acid, dialyzed immediately, dried, and delipidated.
Modification of RNase with Fatty Acids or Glucose-Reaction mix-tures,
in triplicate, were prepared containing 1 mM RNase (equal to 10
mM lysine) and either 100 mM fatty acid or 100 mM glucose in PBS. The
required amounts of fatty acids dissolved in CHCl3 were placed in
sterile 20-ml glass scintillation vials, and the solvent was removed
under a stream of nitrogen passed through a 0.22- m filter. All
subse-quent
additions and the removal of sample aliquots at various times
were conducted using sterile technique in a tissue culture hood.
Solu-tions
of RNase or glucose prepared in sterile PBS were sterilized by
ultrafiltration (0.22- m filter) and added as appropriate to the vials
containing fatty acid. The vials were covered with sterile caps and
placed in a shaking water bath at 37 °C. Aliquots (0.2- 0.4 ml) were
removed at desired times and processed immediately. Fatty acids were
removed by Folch extraction (14). The aqueous layer and protein
inter-face
from the Folch extracts were back-extracted with theoretical Folch
lower phases and dialyzed against water, and the protein was then
processed for measurement of CML. To limit oxidation of FL to CML
during sample hydrolysis, aliquots of protein incubated with glucose
were first reduced with NaBH4 prior to measurement of CML (9).
Recovery of CML in protein incubated with fatty acids only was
unaf-fected
by prior reduction with NaBH4 . In some experiments a second
aliquot (0.7 ml) was used for measurement of glyoxal. Following
acidi-fication
with 25 ml of 3MHCl and the addition of 100 ml of Girard T
reagent (0.5 N) (16), samples were incubated at room temperature for 1
h and then stored at 220 °C; samples were analyzed by HPLC (16) in a
single batch at the end of the experiment.
Protein Hydrolysis and GC/MS Analyses-Following the addition of
d8 -lysine and d8 -CML or 13 C6 -FL internal standards, proteins were
hydrolyzed in 6 N HCl for 24 h at 110 °C. After drying by centrifugal
evaporation, the dried hydrolysates were dissolved in 3 ml of 20%
methanol containing 0.1% trifluoroacetic acid and applied to 3-ml
Sep-Pak
columns (Supelco, Bellefonte, PA) to remove brown and lipophilic
materials prior to derivatization for GC/MS. The eluates were again
dried and then derivatized for measurement of CML or FL by GC/MS as
their trifluoroacetyl methyl ester derivatives (9).
RESULTS
Fig. 1 describes the kinetics of metal-catalyzed oxidation of
normal LDL and concurrent changes in the protein's content of
CML and FL. Comparison of the kinetics of conjugated diene
(panel A) and CML (panel B) formation indicates that the rate
of CML formation parallels the rate of fatty acid peroxidation.
Neither conjugated dienes nor CML increased in the absence of
copper. Because we assumed initially that the CML was de-rived
from oxidation of the Amadori adduct on LDL, the FL
content of the protein was also measured at various stages in
the oxidation reaction. The data in panel C demonstrate unex-pectedly
that, unlike CML, the FL content of LDL remained
constant during the course of the copper oxidation. We con-cluded
tentatively that the CML was being formed from a
product of oxidation of the lipid component of the LDL. To
verify that CML could be formed independent of the presence of
FL, the LDL was reduced with NaBH4 to convert FL to the
inert, redox-inactive hexitollysine adduct. Table I shows that
#5% of the original FL remained on the reduced LDL, yet
following oxidation of the reduced lipoprotein, the yield of CML
was similar to that formed during oxidation of the native pro-tein.
The absorbance traces during metal-catalyzed oxidation of
NaBH4 -reduced LDL were similar to those of the native protein
(data not shown). These results indicate that CML can be
formed on lipoprotein from product(s) of PUFA oxidation.
To further characterize the formation of CML during lipoxi-dation
reactions, model experiments were carried out in which
PUFAs were oxidized in the presence of RNase A, a protein
devoid of carbohydrate. As shown in Fig. 2, oxidation of linole-ate
and arachidonate in the presence of RNase yielded a time-dependent
increase in CML residues in the protein. In these
experiments the fatty acids were progressively solubilized in
buffer as they autoxidized, and the experiments were arbi-trarily
terminated at 6 days when the arachidonate reactions
FIG.1. Copper-catalyzed oxidation of LDL results in an in-crease
in CML without a change in the FL content of the pro-tein.
LDL was incubated with (open symbols) or without (closed sym-bols)
5mMcopper at 32 °C. The progress of the oxidation reaction was
monitored by following conjugated diene formation at 234 nm (A). The
amounts of CML (B) and FL (C) were measured by GC/MS as described
under "Materials and Methods." Data are shown for two different
pools
of LDL.

became a single phase. The overall amount of CML formed was
dependent on the degree of unsaturation and oxidizability of
the fatty acid, with the greatest yield of CML formed from
arachidonate, an intermediate yield from linoleate, and only
trace amounts formed from oleate. The difference in yields of
CML from the various fatty acids probably reflects differences
in their extent of oxidation at the end of the experiment.
Because CML was originally identified as a glycoxidation
product (5, 17), i.e. the result of combined glycation and oxida-tion
reactions, we also compared the relative yield of CML from
glucose and arachidonate. Fig. 3 shows that at the end of 6
days' incubation the yield of CML from autoxidizing arachi-donic
acid, 0.74 6 0.03 mmol/mol RNase, was significantly
greater than that from glucose, 0.03 6 0.003 mmol/mol RNase.
These results indicate that both carbohydrates and lipids may
contribute to formation of CML during autoxidation reactions
in physiological buffer. However, oxidation of fatty acid is
clearly a more efficient source of CML, despite the fact that the
glucose is in solution throughout the course of the experiment,
while the PUFA are only progressively solubilized. Further,
after 6 days of incubation, a large fraction of the arachidonate
was oxidized based on its solubilization in the aqueous phase,
while #2% of the glucose is oxidized during this same time
period (16). Finally, pentosidine, a second glycoxidation prod-uct
known to form during glycoxidation reactions in vitro and
in vivo, was detected in incubations of RNase and glucose, but
no pentosidine was detected either in incubations of RNase
with PUFA or in copper-oxidized LDL.
We have previously shown that glyoxal is both a product of
glucose autoxidation and a source of CML in protein (16).
Glyoxal formation has also been reported during UV irradia-tion
of PUFA (1 and during oxidation of linolenic acid in an
iron ascorbate model system (19, 20), although in the latter
case formation of glyoxal from iron ascorbate itself was not
excluded. In the present experiments the formation of glyoxal
from PUFA was monitored by trapping it as the Girard T
adduct (16). The data in Fig. 4 show that there was a progres-sive
increase in the amount of glyoxal formed in autoxidizing
arachidonic acid incubations, which was not significantly af-fected
by the presence of protein. The data also indicate that
the amount of glyoxal formed during arachidonate oxidation
was more than sufficient to account for the amount of CML
formed on protein, if glyoxal were the only source of all the
CML formed.
DISCUSSION
The observations described above indicate that CML, previ-ously
described as a glycoxidation product or AGE, may, in fact,
be derived from PUFA during lipid peroxidation reactions.
These observations require a reassessment of previous work on
(a) the biochemical origin of AGEs, (b) the significance of
car-bohydrate
oxidation, autoxidative glycosylation, and glycoxida-tion
in the chemical modification of proteins in diabetes, and, in
general, (c) mechanisms of oxidative stress and pathways of
oxidative damage to protein and other biomolecules in aging,
atherosclerosis, and diabetes.
Biochemical Origin of CML-Our studies indicate that lipid
Effect of NaBH4 reduction on formation of FL and CML during
copper oxidation of LDL
Sample Time FL CML
h mmol/mol lysine
Native LDL a 0 0.76-0.80 0.034-0.059
Native LDL a 24 0.76-0.84 0.67-1.09
Reduced LDL b 0 #0.05 0.043-0.077
Reduced LDL b 24 #0.05 0.98-1.1
a LDL was incubated at 32 °C with 5 mM copper, and samples were
removed at indicated times for measurement of FL and CML as de-scribed
under "Materials and Methods." Data are values for two sepa-rate
experiments.
b LDL was reduced with NaBH4 in the presence of 1 mM
diethylene-triaminepentaacetic
acid and then dialyzed against PBS prior to incu-bation
with copper as described above for native LDL. Data are values
for two separate experiments.
FIG.2.CML is formed during incubation of RNase with PUFA.
RNase (1 mM) was incubated with 100 mM arachidonate (E ), linoleate
(M), or oleate (‡ ) in PBS at 37 °C, and aliquots were removed at
indicated times. CML was measured by GC/MS as described under
"Materials and Methods." There was no CML detected in RNase
incu-bated
in the absence of fatty acid. Data (mean 6 S.D.) are for single
measurements of individual aliquots from three separate incubations;
absence of error bars indicates error was within size of symbol.
FIG.3.Comparison of CML formation in RNase from arachi-donate
or glucose. RNase (1 mM) was incubated with 100 mM arachi-donate
(E , replotted from Fig. 2), or 100 mM glucose (‡ ) in PBS. CML
was measured by GC/MS as described under "Materials and Methods."
Data are expressed as described in the legend to Fig. 2.

peroxidation is a potential source of CML during lipoprotein
oxidation and is the major source of CML formed during metal-catalyzed
oxidation of LDL in vitro. Since PUFAs, both in
biological systems and in vitro (Fig. 3) are, in general, more
easily autoxidized in free radical reactions than are carbohy-drates,
it is quite possible that the majority of CML in tissue
proteins is derived from lipid peroxidation reactions, even dur-ing
hyperglycemia when concentrations of glucose and Ama-dori
products on protein are increased. Indeed, the fact that the
FL on LDL was not a significant source of CML formation
during metal-catalyzed oxidation of LDL suggests that glucose
and Amadori adducts may be less important sources of CML in
protein, even in diabetes.
The mechanism of formation of CML and other AGEs during
carbohydrate oxidation reactions is still uncertain. The path-way
may involve oxidation of free glucose or protein-bound
intermediates, including carbinolamine, Schiff base, and Ama-dori
adducts (17, 21, 22). Wells-Knecht et al. (16) identified
glyoxal as one intermediate in the formation of CML from
glucose. Since glyoxal is also formed during peroxidation of
PUFA (Refs. 18-20 and Fig. 4), it may be a common interme-diate
in the formation of CML during oxidation of both carbo-hydrates
and lipids. However, other common intermediates
may also be involved, such as glycolaldehyde (21), a-hydroxy-aldehydes,
or b, g-unsaturated a-hydroxyaldehydes or dicar-bonyls,
which may be formed from both carbohydrate and
PUFA oxidation. The intersection of carbohydrate and lipid
autoxidation reactions in the formation of CML emphasizes the
relationship between the fundamental chemistry and biochem-istry
of these molecules.
Significance of Lipid Peroxidation Reactions in the Maillard
Reaction in Vivo-The importance of lipid peroxidation in the
formation of AGEs and cross-linking of proteins is suggested by
several experimental observations. The browning and cross-linking
of extracellular proteins increase so rapidly in animal
models of diabetes (23) that, in the absence of large endogenous
pools of decompartmentalized transition metal ions, the origin
of the browning products is more readily explained by lipid
rather than carbohydrate oxidation reactions. AGEs also accu-mulate
within a few days on intracellular proteins of cells
grown in high glucose media (24). The rapidity of AGE forma-tion
and the effect of antioxidants as inhibitors of acute glucose
toxicity (25) suggests that they may act by inhibiting glucose-induced
lipid peroxidation reactions (26). Finally, it should be
noted that aminoguanidine, which is a potent inhibitor of
gly-coxidation
reactions in vitro (17, 21), the browning and cross-linking
of collagen in vivo (23), and the development of com-plications
in diabetic animals (3, 4), also inhibits lipid
peroxidation reactions (27-29) Thus, this compound, which has
been described primarily as an inhibitor of advanced glycation
reactions, may in fact be exerting its effects in vivo by inhibi-tion
of lipid peroxidation reactions and/or by trapping of lipid
peroxides and PUFA-derived carbonyl compounds, including
glyoxal.
Mechanisms of Oxidative Stress and Damage in Vivo-Be-cause
similar intermediates may be derived from both carbo-hydrate
and lipid peroxidation reactions, it has become difficult
to discern the primary source of oxidative damage to protein in
complex biological matrices. Palinski et al. (30) have recently
reported, for example, that anti-AGE antibodies detect an in-crease
in AGE epitopes in atherosclerotic plaque in normogly-cemic
animals. Our previous work identifying CML as a major
antigenic determinant in AGE proteins (31) and the present
work identifying CML as a product of lipid peroxidation sug-gest
that the increase in AGE epitopes in atherosclerotic
plaque could result from an increase in CML derived from lipid
peroxidation reactions. In addition, lipid-derived CML may
also be the major AGE epitope accumulating in intracellular
protein in endothelial cells exposed to glucose-induced oxida-tive
stress (24).
To distinguish carbohydrate- from lipid-mediated damage
and assess the relative importance of oxidation of these two
substrates in the development of diabetic complications, it will
be necessary to identify unique products derived from each of
these precursors. In the meantime, since CML has been iden-tified
as a major AGE antigen in tissue proteins and a product
of both carbohydrate and lipid peroxidation reactions, our re-sults
suggest that CML may be more useful as a general bi-omarker
of oxidative stress and damage in tissue proteins.
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Biology and
Medicine, 2nd Ed., Clarendon Press, Oxford
2. Witztum, J. L., and Steinberg, D. (1991) J. Clin. Invest. 88,
1785-1792
3. Brownlee, M. (1994) Diabetes 43, 836-841
4. Vlassara, H., Bucala, R., and Striker, L. (1994) Lab. Invest. 70,
138-151
5. Baynes, J. W. (1991) Diabetes 40, 405-412
6. Curtiss, L. K., and Witztum, J. L. (1985) Diabetes 34, 452-461
7. Mullarkey, C. J., Edelstein, D., and Brownlee, M. (1990) Biochem.
Biophys.
Res. Commun. 173, 932-939
8. Tsai, E. C., Hirsch, I. B., Brunzell, J. D., and Chait, A. (1994)
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9. Knecht, K. J., Dunn, J. A., McFarland, K. F., McCance, D. R., Lyons,
T. J.,
Thorpe, S. R., and Baynes, J. W. (1991) Diabetes 40, 190-196
10. Chung, B. H., Segrest, J. P., Ray, M. J., Brunzell, J. D.,
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Krauss, R. M., Beudrie, K., and Cone, J. T. (1986) Methods Enzymol.
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Chem. 226,
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15. Deleted in proof
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and Baynes,
J. W. (1995) Biochemistry 34, 3702-3709
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R., and
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Biochemistry 34,
FIG.4. Glyoxal formation from arachidonic acid. Aliquots of
reaction mixtures containing either arachidonate alone (E ) or
ararchi-donate
and RNase (M) were removed at indicated times, and glyoxal
was measured by HPLC as described under "Materials and Methods."
Data are the average 6 range for two separate experiments. For
com-parison
the data from Fig. 2 for CML formation from arachidonate (l),
expressed as mM, are also shown; absence of error bars indicates error
was within size of symbol.

If you have raised blood sugar levels your chances of developing
Alzheimer's disease are higher, say researchers from the Karolinska
Institute, Stockholm, Sweden.

Researchers presented their finding yesterday at the Alzheimer's
Conference, Madird, Spain. The study looked at over 1,173 people, aged
75 - some of whom had developed dementia, while others had not.

Previous studies have identified an association between diabetes type 2
and Alzheimer's risk. In this study, the researchers sought to examine
the hypothesis that borderline diabetes mellitus (pre-diabetes) is a
risk factor for dementia and Alzheimer disease.

This new research indicates the risk is also there for people who have
raised blood sugar levels, but have not yet developed diabetes type 2 -
people with pre-diabetes. The link is stronger if the person has
pre-diabetes together with severe systolic hypertension (high blood
pressure).

Many more people have pre-diabetes than those with diabetes type 2. In
the USA 14.6 million people have diabetes, while it is estimated that
about 41 million are in the pre-diabetes category.

The prevalence of Alzheimer's disease is expected to increase as people
live longer and more people develop diabetes over the coming decades.
According to the findings of this new research, Alzheimer's rates may
go up even faster than was previously thought.

What is sugar diabetes exactly? Is this a new disease you have
discovered?

That is what it was first called during the time of the ancient greeks
and it should very aptly still be called.

TC

Interesting that you are smart enough to realize that fat does not
cause heart disease but food that is not real as you would say (trans
fat, etc) Suprising you have not woken up to the same realization
about sugar.

Are you saying that sugar is real food and that it is healthy for you?

If you have raised blood sugar levels your chances of developing
Alzheimer's disease are higher, say researchers from the Karolinska
Institute, Stockholm, Sweden.

Researchers presented their finding yesterday at the Alzheimer's
Conference, Madird, Spain. The study looked at over 1,173 people, aged
75 - some of whom had developed dementia, while others had not.

Previous studies have identified an association between diabetes type 2
and Alzheimer's risk. In this study, the researchers sought to examine
the hypothesis that borderline diabetes mellitus (pre-diabetes) is a
risk factor for dementia and Alzheimer disease.

This new research indicates the risk is also there for people who have
raised blood sugar levels, but have not yet developed diabetes type 2 -
people with pre-diabetes. The link is stronger if the person has
pre-diabetes together with severe systolic hypertension (high blood
pressure).

Many more people have pre-diabetes than those with diabetes type 2. In
the USA 14.6 million people have diabetes, while it is estimated that
about 41 million are in the pre-diabetes category.

The prevalence of Alzheimer's disease is expected to increase as people
live longer and more people develop diabetes over the coming decades.
According to the findings of this new research, Alzheimer's rates may
go up even faster than was previously thought.

What is sugar diabetes exactly? Is this a new disease you have
discovered?

That is what it was first called during the time of the ancient greeks
and it should very aptly still be called.

TC

Interesting that you are smart enough to realize that fat does not
cause heart disease but food that is not real as you would say (trans
fat, etc) Suprising you have not woken up to the same realization
about sugar.

If you have raised blood sugar levels your chances of developing
Alzheimer's disease are higher, say researchers from the Karolinska
Institute, Stockholm, Sweden.

Researchers presented their finding yesterday at the Alzheimer's
Conference, Madird, Spain. The study looked at over 1,173 people, aged
75 - some of whom had developed dementia, while others had not.

Previous studies have identified an association between diabetes type 2
and Alzheimer's risk. In this study, the researchers sought to examine
the hypothesis that borderline diabetes mellitus (pre-diabetes) is a
risk factor for dementia and Alzheimer disease.

This new research indicates the risk is also there for people who have
raised blood sugar levels, but have not yet developed diabetes type 2 -
people with pre-diabetes. The link is stronger if the person has
pre-diabetes together with severe systolic hypertension (high blood
pressure).

Many more people have pre-diabetes than those with diabetes type 2. In
the USA 14.6 million people have diabetes, while it is estimated that
about 41 million are in the pre-diabetes category.

The prevalence of Alzheimer's disease is expected to increase as people
live longer and more people develop diabetes over the coming decades.
According to the findings of this new research, Alzheimer's rates may
go up even faster than was previously thought.

If you have raised blood sugar levels your chances of developing
Alzheimer's disease are higher, say researchers from the Karolinska
Institute, Stockholm, Sweden.

Researchers presented their finding yesterday at the Alzheimer's
Conference, Madird, Spain. The study looked at over 1,173 people, aged
75 - some of whom had developed dementia, while others had not.

Previous studies have identified an association between diabetes type 2
and Alzheimer's risk. In this study, the researchers sought to examine
the hypothesis that borderline diabetes mellitus (pre-diabetes) is a
risk factor for dementia and Alzheimer disease.

This new research indicates the risk is also there for people who have
raised blood sugar levels, but have not yet developed diabetes type 2 -
people with pre-diabetes. The link is stronger if the person has
pre-diabetes together with severe systolic hypertension (high blood
pressure).

Many more people have pre-diabetes than those with diabetes type 2. In
the USA 14.6 million people have diabetes, while it is estimated that
about 41 million are in the pre-diabetes category.

The prevalence of Alzheimer's disease is expected to increase as people
live longer and more people develop diabetes over the coming decades.
According to the findings of this new research, Alzheimer's rates may
go up even faster than was previously thought.

If you have raised blood sugar levels your chances of developing
Alzheimer's disease are higher, say researchers from the Karolinska
Institute, Stockholm, Sweden.

Researchers presented their finding yesterday at the Alzheimer's
Conference, Madird, Spain. The study looked at over 1,173 people, aged
75 - some of whom had developed dementia, while others had not.

Previous studies have identified an association between diabetes type 2
and Alzheimer's risk. In this study, the researchers sought to examine
the hypothesis that borderline diabetes mellitus (pre-diabetes) is a
risk factor for dementia and Alzheimer disease.

This new research indicates the risk is also there for people who have
raised blood sugar levels, but have not yet developed diabetes type 2 -
people with pre-diabetes. The link is stronger if the person has
pre-diabetes together with severe systolic hypertension (high blood
pressure).

Many more people have pre-diabetes than those with diabetes type 2. In
the USA 14.6 million people have diabetes, while it is estimated that
about 41 million are in the pre-diabetes category.

The prevalence of Alzheimer's disease is expected to increase as people
live longer and more people develop diabetes over the coming decades.
According to the findings of this new research, Alzheimer's rates may
go up even faster than was previously thought.